Li Duan, Mabrouk Omar S, Liu Tiecheng, Tian Fangyun, Xu Gang, Rengifo Santiago, Choi Sarah J, Mathur Abhay, Crooks Charles P, Kennedy Robert T, Wang Michael M, Ghanbari Hamid, Borjigin Jimo
Departments of Molecular and Integrative Physiology.
Chemistry, Pharmacology.
Proc Natl Acad Sci U S A. 2015 Apr 21;112(16):E2073-82. doi: 10.1073/pnas.1423936112. Epub 2015 Apr 6.
The mechanism by which the healthy heart and brain die rapidly in the absence of oxygen is not well understood. We performed continuous electrocardiography and electroencephalography in rats undergoing experimental asphyxia and analyzed cortical release of core neurotransmitters, changes in brain and heart electrical activity, and brain-heart connectivity. Asphyxia stimulates a robust and sustained increase of functional and effective cortical connectivity, an immediate increase in cortical release of a large set of neurotransmitters, and a delayed activation of corticocardiac functional and effective connectivity that persists until the onset of ventricular fibrillation. Blocking the brain's autonomic outflow significantly delayed terminal ventricular fibrillation and lengthened the duration of detectable cortical activities despite the continued absence of oxygen. These results demonstrate that asphyxia activates a brainstorm, which accelerates premature death of the heart and the brain.
在缺氧情况下健康心脏和大脑迅速死亡的机制尚未完全明了。我们对经历实验性窒息的大鼠进行了连续心电图和脑电图监测，并分析了核心神经递质的皮质释放、脑和心脏电活动的变化以及脑-心连接性。窒息刺激功能性和有效皮质连接性出现强烈且持续的增加、大量神经递质的皮质释放立即增加，以及皮质-心脏功能性和有效连接性的延迟激活，这种激活一直持续到心室颤动发作。尽管持续缺氧，但阻断大脑的自主神经传出显著延迟了终末期心室颤动，并延长了可检测到的皮质活动持续时间。这些结果表明，窒息激活了一场“头脑风暴”，加速了心脏和大脑的过早死亡。
